Synergistic effects of nitric oxide and prostaglandins on renal escape from vasopressin-induced antidiuresis

Murase, Takashi; Tian, Ying; Fang, Xiaojun; Verbalis, Joseph G.

doi:10.1152/ajpregu.00065.2002

Cited by 24 publications

(21 citation statements)

References 32 publications

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“…On the other hand, AVP infusion stimulates aquaporin-2 apical membrane expression in renal collecting ducts under physiological conditions, although modulation of this process after endotoxin challenge is unknown. "Vasopressin escape" from antidiuresis has been described in animals after several days of drug infusion and is related (6) to a marked AVP-independent decrease in kidney aquaporin-2 mRNA and protein expression as well as AVP V2 receptor binding (18,29). In this study natriuresis did not increase after endotoxin challenge and AVP infusion, but the experimental period was very short.…”

Section: Effects Of Drug Treatment On Diuresis and Renal Functionmentioning

confidence: 57%

Comparative effects of vasopressin, norepinephrine, and l-canavanine, a selective inhibitor of inducible nitric oxide synthase, in endotoxic shock

Lévy

Vallée²,

Lauzier³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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. Comparative effects of vasopressin, norepinephrine, and L-canavanine, a selective inhibitor of inducible nitric oxide synthase, in endotoxic shock. Am J Physiol Heart Circ Physiol 287: H209 -H215, 2004. First published February 26, 2004 10.1152/ajpheart.00946.2003, a standard of care, AVP, an alternative candidate, and L-canavanine (LC), a selective inhibitor of inducible nitric oxide synthase, were compared for efficacy and innocuousness on global and regional hemodynamics, plasmatic and tissue lactate-to-pyruvate ratio (L/P), tissue high-energy phosphates, renal function, and tissue capillary permeability in a rat model of endotoxic normokinetic shock. Mean arterial pressure (MAP) decreased (ϳ35%) but aortic blood flow increased during endotoxin infusion (P Ͻ 0.05 vs. control). Additionally, there was a decrease in mesenteric (MBF) and renal (RBF) blood flows along with regional-to-systemic ratio (P Ͻ 0.05 vs. control). All tested drugs restored MAP to basal levels but slightly decreased abdominal aortic flow; however, RBF and MBF remained unchanged. Endotoxin significantly decreased diuresis and inulin clearance (ϳ3-to 4-fold), whereas AVP or LC attenuated this drop (P Ͻ 0.05 vs. control). In contrast, NE did not improve endotoxininduced renal dysfunction. Endotoxin induced gut and lung hyperpermeability (P Ͻ 0.05 vs. control). Endotoxin-induced gut hyperpermeability was inhibited by AVP, LC, and NE. Endotoxin-induced lung hyperpermeability was further worsened by NE (ϳ2-fold increase) but not AVP infusion (P Ͻ 0.05 vs. endotoxin). LC significantly improved endotoxin-induced pulmonary hyperpermeability. Endotoxin increased renal lactate and decreased renal ATP. NE did not change renal lactate or renal ATP. AVP and LC decreased renal lactate and normalized renal ATP. Finally, endotoxin was associated with increased lactate levels and L/P (ϳ2-and 1.5-fold increases vs. control, respectively), whereas AVP and LC, but not NE, normalized both parameters after endotoxin challenge. These results suggest that, in a short-term endotoxic shock model, AVP improves systemic hemodynamics without side effects and has particular beneficial effects on renal function. septic shock; vascular permeability; renal function THE HUMAN RESPONSE to septic challenge usually includes increased cardiac output, decreased peripheral resistance, low arterial pressure, and increased vascular permeability. AVP, also known as "the" antidiuretic hormone (ADH), is an emerging alternative candidate for management of redistributive shock (7). Indeed, AVP exhibits strong vasoconstrictor effects through stimulation of the V1 receptor leading to arterial pressure improvement (28). Moreover, low concentrations of exogenous AVP mediate vasodilatation in coronary, cerebral, and pulmonary arterial circulation (20). The recognized effects of AVP on renal function are complex and include association of an antidiuretic effect through stimulation of V2 receptors, an increase of diuresis/natriuresis through V1 receptors by efferent arteriolar vasoconstric...

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Section: Effects Of Drug Treatment On Diuresis and Renal Functionmentioning

confidence: 57%

Comparative effects of vasopressin, norepinephrine, and l-canavanine, a selective inhibitor of inducible nitric oxide synthase, in endotoxic shock

Lévy

Vallée²,

Lauzier³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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“…Inhibition of nitric oxide and prostaglandin synthesis was able to increase aquaporin 2 level and therefore avoid the vasopressin escape phenomenon (24). Several experimental studies have indicated that angiotensin II (AngII) can increase V 2 R expression, so the low AngII concentration observed in SIADH could contribute to the escape (25).…”

Section: Urine Osmolalitymentioning

confidence: 99%

Clinical Laboratory Evaluation of the Syndrome of Inappropriate Secretion of Antidiuretic Hormone

Decaux

Musch²

2008

Clinical Journal of the American Society of Nephrology

145

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Hyponatremia secondary to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is a frequent cause of hypotonicity. Although the differential diagnosis with other causes of hypotonicity such as salt depletion is sometimes challenging, some simple and readily available biologic parameters can be helpful in the diagnosis of SIADH. In SIADH, urea is typically low; this is less specific for elderly patients, for whom lower clearance of urea accounts for higher values. Low levels of uric acid are more often seen in SIADH (70%) compared with salt-depleted patients (40%). Typically, patients with SIADH will show a lower anion gap with nearly normal total CO 2 and serum potassium, this despite dilution. In patients with hyponatremia secondary to hypocorticism, total CO 2 is usually lower than in nonendocrine SIADH despite low urea and uric acid levels. Urine biology can also be helpful in diagnosis of SIADH because patients with SIADH have high urine sodium (Na; >30 mEq/L), and most of them will have a high fractional excretion of Na (>0.5% in 70% of cases), reflecting salt intake. Conversely, low urine Na in patients with SIADH and poor alimentation is not rare. Finally, measurement of urine osmolality is useful for the diagnosis of polydipsia and reset osmostat and could further help in the choice of therapeutic strategy because patients with low urine osmolality will benefit from water restriction or urea, whereas those with high urine osmolality (>600 mOsm/kg) would be good candidates for V 2 antagonist.

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“…However, it is now clear that vasopressin-independent pathways also play a role, since decreases in AQP2 are seen in association with the ability to lose water in the urine despite ongoing vasopressin infusion (vasopressin escape phenomenon) (8,9). This escape phenomenon has been shown to depend on both nitric oxide and prostaglandin production (26). There is evidence that tonicity may be a significant signal (16,19).…”

mentioning

confidence: 99%

Dehydration-induced increase in aquaporin-2 protein abundance is blocked by nonsteroidal anti-inflammatory drugs

Baggaley

Nielsen

Marples

2010

American Journal of Physiology-Renal Physiology

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It is now well established that the antidiuretic response to vasopressin is modulated by changes in aquaporin-2 (AQP2) expression in response to hydration status. While vasopressin itself is one signal driving expression, other signals also play a part. In this study, we planned to investigate whether prostaglandins, known to modulate AQP2 trafficking, may play a role in this process. Male Wistar rats were kept in metabolic cages, with either free access to water and food, or were given 15 g of food gelled with water, such that they were fluid restricted or fluid loaded. The effects of oral administration of two structurally different NSAIDs, indomethacin and ibuprofen, and a COX-2-selective NSAID, meloxicam, on urine output and AQP2 expression were investigated in kidneys removed under terminal anesthesia. All the NSAIDs decreased AQP2 expression significantly in water-restricted rats but did not significantly alter PGE excretion. In water-loaded rats, the effects were less marked, and meloxicam had no significant effect. Consistent with this, ibuprofen prevented the increase in AQP2 expression seen in response to dehydration. These results demonstrate that NSAIDs decrease AQP2 protein abundance, particularly during adaptation during dehydration. This may be of particular significance in older and critically ill patients, who are prone to dehydration.antidiuresis; vasopressin; collecting duct IT IS NOW WELL ESTABLISHED that the acute antidiuretic action of vasopressin depends on the exocytic insertion of aquaporin-2 (AQP2) water channels from a store in intracellular vesicles to the apical plasma membrane of collecting duct principal cells (13,24,29,34), the so-called "shuttle" mechanism. Furthermore, there is now clear evidence that this acute response is modulated by changes in the total amount of AQP2 present in the cells. Such changes occur in response to chronic alterations in hydration, with water loading causing a decrease in AQP2 expression, while dehydration increases the AQP2 levels (28). Changes in AQP2 expression are also found in association with a variety of pathological conditions associated with either excess water loss (1,7,11,12,23,25) or water retention (2,30,31,39).The signals associated with changes in AQP2 expression are currently being sought. One signal is vasopressin, which causes an increase in AQP2 expression when given as a chronic infusion to either Brattleboro rats (which lack endogenous vasopressin) (5) or normal rats (8,9). This effect is thought to be mediated by cAMP and protein kinase A, which also plays a pivotal role in the acute shuttling response, via phosphorylation of a CRE-binding protein, which then binds to the promoter of the AQP2 gene (38). However, it is now clear that vasopressin-independent pathways also play a role, since decreases in AQP2 are seen in association with the ability to lose water in the urine despite ongoing vasopressin infusion (vasopressin escape phenomenon) (8, 9). This escape phenomenon has been shown to depend on both nitric oxide and prostagl...

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Synergistic effects of nitric oxide and prostaglandins on renal escape from vasopressin-induced antidiuresis

Cited by 24 publications

References 32 publications

Comparative effects of vasopressin, norepinephrine, and l-canavanine, a selective inhibitor of inducible nitric oxide synthase, in endotoxic shock

Comparative effects of vasopressin, norepinephrine, and l-canavanine, a selective inhibitor of inducible nitric oxide synthase, in endotoxic shock

Clinical Laboratory Evaluation of the Syndrome of Inappropriate Secretion of Antidiuretic Hormone

Dehydration-induced increase in aquaporin-2 protein abundance is blocked by nonsteroidal anti-inflammatory drugs

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